Health and metabolic responses of young calves housed at -30 degrees C to -8 degrees C.

Newborn, male, Holstein calves, were continuously housed for three weeks in calf hutches at 17 degrees C or in a thermal environment which varied rhythmically on a daily basis either between -20 degrees C and -8 degrees C (experiment A) or between -30 degrees C and -18 degrees C (experiment B). Compared to warm-housed calves, cold-housed calves in experiment A had metabolic rates which were significantly higher (p less than 0.001) in a standing position but which were not significantly different (p less than 0.05) in a recumbent position. Recumbent and standing cold-housed calves in experiment B had an increased (p less than 0.05) metabolic rate compared to warm-housed controls. Heat loss was less (p less than 0.05) for recumbent cold-housed calves in experiment B than for standing calves in a thermoneutral environment. Localized subcutaneous hemorrhages of hindlimbs were a consistent necropsy finding among all cold-housed calves. Average daily gains of cold-housed calves were not significantly different from warm-housed controls. Clinical, physiological and pathological findings indicated that cold treatments used in the present study did not cause serious harm to calves. It was concluded that calves housed in properly managed hutches are remarkably cold tolerant.

Thermal insulation of young calves exposed to cold.

Tissue, external and whole animal insulation values were determined for 12 newborn male Holstein calves continuously housed for two weeks in hutches within environmental chambers in which temperature was maintained at a constant 17 degrees C (three calves) or cycled on a daily basis either between -20 degrees and -8 degrees C (three calves) or between -30 degrees and -18 degrees C (six calves). Three of the six calves at the coldest temperature were outfitted with an insulated coat. The insulated coat provided calves a 52% increase in total insulation. Tissue insulation of cold-housed calves increased 37.2% over the first two weeks of life. It was concluded that the capacity for vasoconstriction improved with age. External insulation did not change significantly except during the first week in cold-housed calves without insulated coats. External insulation values were five to eight times those of tissue insulation values for all treatment groups. This indicated that insulation of structures external to the skin (hair, bedding, ground, etc.) provided most of the insulation for calves.

Monoamine oxidase inhibition and furazolidone-induced cardiomyopathy in turkey poults.

Furazolidone (FZ), a potent inhibitor of monoamine oxidase (MAO), fed at concentrations of 700 ppm to turkey poults 2 through 5 weeks of age, produces cardiomyopathy and cardiomegaly. To determine the role of MAO inhibition in FZ-induced cardiomyopathy, the effects of FZ were compared with those of a chemically different MAO inhibitor, tranylcypromine (TCP), and a chemically similar non-MAO inhibitor, nitrofurazone (NFZ). At 14 days of age, poults were divided randomly into four groups. Control poults were fed a standard turkey starter ration, and poults in the experimental groups were fed the standard ration that included one of the following drugs at the given concentrations: 700 ppm FZ, 350 ppm NFZ, or 50 ppm TCP. Activity of MAO was assayed in liver and kidney homogenates from poults chosen at random at 14, 17, 21, 28, and 35 days of age in one trial and on heart homogenates at 14, 15, 17, 19, and 28 days of age in another trial. Development of cardiomyopathy was assessed using an electrocardiographic (ECG) technique and substantiated with necropsy examination. Inhibition of MAO was observed only in the heart in FZ-fed poults, only in the kidney in NFZ-fed poults, and in all three tissues studied in TCP-fed poults. Under the conditions of this study, an increase in the incidence of cardiomyopathy, based on ECG data and necropsy results, occurred only in the FZ-fed group. The inability of the potent MAO inhibitor, TCP, to produce cardiomyopathy in this study supports the conclusion that the primary mechanism of FZ-induced cardiomyopathy in turkey poults is probably not due to MAO inhibition.

Effect of furazolidone on plasma enzyme and protein levels in turkey poults.

Furazolidone (FZ) at a dose of 700 ppm was fed to turkey poults beginning at 2 weeks of age. In trial 1, plasma collected by venipuncture was assayed for glutamic oxalacetic transaminase (GOT), lactate dehydrogenase (LDH), and total protein at 19, 23, 26, and 30 days of age. Significant (P less than or equal to .05) differences were noted only in levels of plasma LDH, which were elevated in FZ-fed poults at all stages studied. In Trial 2, plasma collected by venipuncture was assayed for creatine phosphokinase (CPK), GOT, glutamic pyruvic transaminase (GPT), and LDH daily from 15 through 19 days of age and for protein at 19 days of age. Significant elevations (P less than or equal to .05) were noted in levels of plasma a) CPK at 15 days, b) GOT at 18 days, and c) LDH at 17 and 19 days. A significant (P less than or equal to .01) depression in plasma protein was observed at 19 days. Plasma GPT was either absent or present in very low concentrations. These data suggest that FZ exerts its primary effect on the myocardium. THe initial myocardial changes occur prior to their detection by known electrocardiographic (ECG) technics.

The production of cardiomyopathy in turkey poults by the oral administration of furazolidone.

Furazolidone (FZ) was given to turkey poults two weeks post-hatching by stomach tube in doses of 60 and 80 mg/kg per day, and via the feed at a concentration of 700 ppm. Oral doses were given either as one dose at 8 a.m. or as two equal doses given at 8 a.m. and 4 p.m. Electrocardiographic (ECG) recordings were used to monitor the development of round-heart disease (RHD) and necropsies were performed on all poults to corroborate the ECG findings. All poults receiving FZ gained significantly less weight (p less than or equal to .05) than control poults. At oral doses of 80 mg/kg per day, the apparent acute toxicity of FZ resulted in high mortality during the first week of the experiment. At necropsy there were no signs of RHD in these poults. Most of the poults given FZ orally in doses of 60 mg/kg per day or at 700 ppm in the feed survived to the termination of the experiments. The majority of these poults showed ECG patterns that are typical of RHD. Myocardial lesions indicative of RHD were present at necropsy.

Electrocardiographic technic for identifying developing cardiomyopathies in young turkey poults.

A modification of the technic for the utilization of electrocardiographic (ECG) data to identify round heart poults was used to screen poults with questionable ECG recordings and to diagnose poults with early cardiomyopathies. In two experimental trials, using a voltage greater than .1 mV (NH) in the R wave of Lead I as a criterion, it was possible trom 20 to 24%. At subsequent periodic data gathering, 37% of the poults in Trial I and 27% of the poults in Trial II exhibited NH before developing the typical normal transitional to round heart (NT leads to R) ECG pattern of the round heart syndrome. Necropsy findings confirmed myocardial alterations in a majority of the poults with NH whether or not the typical round heart ECG pattern ensued. Application of this finding is discussed.